Placenta · 2026
Evaluation on the significance of miR-338-3p for preterm premature rupture of membranes with histologic chorioamnionitis.
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Liu Rong, Li Yang, Fu Fan, Yu Juan
Аннотация
BACKGROUND: Preterm premature rupture of membranes (PPROM) before full term can lead to adverse pregnancy outcomes. Chorioamnionitis is the main cause of premature birth. This investigation aims to evaluate the clinical value of miR-338-3p in PPROM with histological chorioamnionitis (HCA), and its mechanism in human amniotic epithelial cells (hAECs).
METHODS: 215 patients with PPROM were included (PPROM-HCA group (n = 105), PPROM group (n = 110)). MiR-338-3p and PTN expression in the tissues were measured via real time quantitative polymerase chain reaction. The diagnostic value of miR-338-3p for PPROM with HCA was evaluated using receiver operating characteristic analysis. Cell proliferation, apoptosis and inflammatory factor levels were quantified via cell counting kit-8, flow cytometry and enzyme-linked immunosorbent assay.
RESULTS: Compared with PPROM group, miR-338-3p was upregulated in the tissues of PPROM-HCA patients, while PTN was downregulated. MiR-338-3p had a good diagnostic value for PPROM-HCA patients. MiR-338-3p overexpression suppressed hAECs proliferation, promoted apoptosis, and increased interleukin-6 and tumor necrosis factor-α levels; inhibition of miR-338-3p showed the reverse phenotypes. PTN was the target gene of miR-338-3p. PTN overexpression partially reversed the cell proliferation inhibition, increased apoptosis and release of inflammatory factors induced by the upregulation of miR-338-3p.
CONCLUSION: MiR-338-3p is upregulated in PPROM-HCA patients, and it has a good diagnostic value. MiR-338-3p modulates the proliferation, apoptosis and inflammatory response of hAECs via targeting PTN. These findings offer novel insights into the pathological research of PPROM-HCA.
METHODS: 215 patients with PPROM were included (PPROM-HCA group (n = 105), PPROM group (n = 110)). MiR-338-3p and PTN expression in the tissues were measured via real time quantitative polymerase chain reaction. The diagnostic value of miR-338-3p for PPROM with HCA was evaluated using receiver operating characteristic analysis. Cell proliferation, apoptosis and inflammatory factor levels were quantified via cell counting kit-8, flow cytometry and enzyme-linked immunosorbent assay.
RESULTS: Compared with PPROM group, miR-338-3p was upregulated in the tissues of PPROM-HCA patients, while PTN was downregulated. MiR-338-3p had a good diagnostic value for PPROM-HCA patients. MiR-338-3p overexpression suppressed hAECs proliferation, promoted apoptosis, and increased interleukin-6 and tumor necrosis factor-α levels; inhibition of miR-338-3p showed the reverse phenotypes. PTN was the target gene of miR-338-3p. PTN overexpression partially reversed the cell proliferation inhibition, increased apoptosis and release of inflammatory factors induced by the upregulation of miR-338-3p.
CONCLUSION: MiR-338-3p is upregulated in PPROM-HCA patients, and it has a good diagnostic value. MiR-338-3p modulates the proliferation, apoptosis and inflammatory response of hAECs via targeting PTN. These findings offer novel insights into the pathological research of PPROM-HCA.